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Results: There were no significant differences between the two groups regarding age, sex, body surface area, history of hypertension, or diameter of the ascending aorta before surgery. Four patients in group AD had gene-related aortic dissection (Marfan syndrome, three patients; bicuspid aortic valve, one patient). Nine patients in group AA had a bicuspid aortic valve. There were significant differences between the two groups in regard to smooth muscle cell proliferation [VV (group AD: 1.40 ± 0.49 points; group AA: 0.98 ± 0.19 points; p<0.001); VVV (group AD: 1.40 ± 0.55 points, group AA: 1.04 ± 0.51 points, p=0.013] and total degeneration score (VV: group AD: 3.17 ± 1.42 points, group AA: 2.39 ± 1.41 points, p=0.036). There were no significant differences between the two groups regarding myomatous change or sclerosis.

Conclusions: Degeneration of the VV and, especially, smooth muscle cell proliferation of the VV and VVV appear to be responsible for aortic dissection. Elucidation of the smooth muscle degeneration pathway may lead to identifying the turning point at which aortic wall weakness induces dissection or enlargement.